Depression of Ventricular Contractility by Stimulation of the Vagus Nerves

Degeest, H; Levy, Matthew N.; Zieske, Harrison; Lipman, Ralph I.

doi:10.1097/00132586-196604000-00006

Cited by 31 publications

(42 citation statements)

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“…3) On the other hand, after dextran infusion the stroke work of the left ventricle is 65 g-m per beat per m2 with a LVEDP of 16 mm Hg, whereas after atropine the stroke work is 67 g-m per beat per m2 with a LVEDP of 10 mm Hg (86). This enhancement of the left ventricular performance may be interpreted-especially on the basis of some recent evidence of a tonic negative inotropic influence of the vagus nerves upon mammalian ventricular myocardium (87,88)-as the result of the parasympatholytic activity of the drug on the ventricle, and it may be considered at the origin of the pressure decrease which, in turn, may interrupt the reflex mechanism suggested above. Finally, 4) it cannot be excluded that the fall of end-diastolic pressure of both ventricles after atropine (86) is due to peripheral and splanchnic venous pooling of blood, with consequent relief of heart congestion and improvement of ventricular function, but Horsley and Eckstein found diminished forearm venous volume and increased venous tone after intravenous injection of 2 mg of atropine sulfate in normal subjects; this response was not altered after inflation of an antigravity suit over the abdomen and the lower limbs (89).…”

Section: Discussionmentioning

confidence: 93%

Pulmonary vascular distensibility and lung compliance as modified by dextran infusion and subsequent atropine injection in normal subjects.

Giuntini¹,

Maseri²,

Bianchi³

1966

J. Clin. Invest.

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Little information is available on the pressurevolume relationship of the human pulmonary circulation. Observations have been almost exclusively confined to limited groups of cardiac patients (1-6) in whom coexistence of extravascular alterations, such as interstitial perivascular edema (7, 8), may hinder the interpretation of the results. On the other hand, extrapolation to man of animal studies on the pressure-volume characteristics of the whole pulmonary vascular bed or part of it is not always warranted because of species variation and wide experimental differences. Finally, the combined evaluation of pulmonary vascular resistance and transmural pressure may provide information on the distensibility of resistive vessels but does not allow deductions on the distensibility of the pulmonary circulation as a whole, since the distribution of volume does not parallel that of resistance.Previous reports have shown that the infusion of a plasma expander raised the pulmonary arterial and wedge pressures to the same extent (9); if the change in pressure was assumed to be practically uniform throughout the bed, such an infusion seemed to provide an opportunity to assess the compliance of the pulmonary vascular bed by determining the ratio of the change in volume to the change in pressure.The values of the distensibility of the pulmonary circulation obtained with dextran infusion during the first studies were thought to be exceedingly low. We then decided to test some drug that could enhance the distensibility of the pulmonary vascular bed. Atropine sulfate, which was

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Section: Discussionmentioning

confidence: 93%

Pulmonary vascular distensibility and lung compliance as modified by dextran infusion and subsequent atropine injection in normal subjects.

Giuntini¹,

Maseri²,

Bianchi³

1966

J. Clin. Invest.

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“…Possibly the same stimulus that caused the more substantial change in HR also affected other factors that may directly influence SV, such as afterload, diastolic filling, or myocardial contractility. For ex-ample, a vagal response includes bradycardia, increased vascular resistance, and decreased contractility (22) and is a possible explanation for the considerable decrease in both HR and SV.…”

Section: Discussionmentioning

confidence: 99%

Relationship between Heart Rate, Left Ventricular Output, and Stroke Volume in Preterm Infants during Fluctuations in Heart Rate

Winberg

Ergander

1992

Pediatr Res

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ABSTRACT. The relationship between changes in heart rate, left ventricular output, and left ventricular stroke volume was studied in 18 preterm infants, with mean gestational age 29 wk (range 26-33 wk) and mean postnatal age 10 d (range 1-21 d). To yield left ventricular output, the blood flow velocity in the ascending aorta was measured by range-gated Doppler technique and multiplied by the aortic cross-sectional area measured by cross-sectional and M-mode echocardiography. Stroke volume was calculated by dividing left ventricular output by heart rate. The individual mean left ventricular output correlated poorly with heart rate ( 3 = 0.17), and, accordingly, there was a closer relationship between stroke volume and left ventricular output. In only four of the 18 infants was a significant correlation between heart rate changes and left ventricular output found. Substantial changes in stroke volume were seen in most infants, and in 1 3 of the 18 infants the changes exceeded 25%. These variations in stroke volume were closely related to left ventricular output. In 15 of the 18 infants, the maximum heart rate change was associated with a stroke volume change in the opposite direction. The group average of the maximum heart rate increase in each individual, 24 bpm (18%), corresponded to a decrease in stroke volume of 0.15 mL.kg-' (9%) (p < 0.05) and an increase in left ventricular output of 22.7 m L min-' .kg-' (9%) (p < 0.05). A reciprocal relationship was seen between afterload and left ventricular output. The findings indicate that the preterm infant has a substantial ability to alter stroke volume and that stroke volume is an important determinant of neonatal left ventricular output. During beat-to-beat fluctuations in heart rate, the stroke volume changes appear to reduce the effect of the heart rate changes on output. (Pediatr Res 31: 117-120,1992 Supported by the Karolinska Institute, the General Maternity Hospital Foundation, the Swedish Society for Medicine, and Sallskapet Barnavird.Studies of the fetal and neonatal heart have provided basic information about the myocardial immaturity on the cellular and subcellular levels. The immature myocardium has been shown to contain more water, less contractile elements per unit weight, and less sarcoplasmic reticulum (1, 2). Furthermore, the cardiac sympathetic innervation is not fully developed at birth (3, 4). In in vitro experiments these differences correspond to reduced compliance and reduced contractile force (1) compared with the mature myocardium. However, the hemodynamic consequences of the myocardial immaturity on the intact circulatory system are, despite extensive investigations, still not clearly delineated. It has been claimed that the fetal heart performs at or near its peak capacity even during normal conditions and has a very limited ability to change (SV) (5, 6). Accordingly, fetal and neonatal cardiac output should be almost entirely dependent on HR. This, however, has been questioned in other fetal and neonatal lamb studies (7-lo), as well as in...

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“…3 H-cyclic AMP (specific activity 37.7 c/mmole) was purchased from New England Nuclear Corporation. I-Sc-cyclic GMP (specific activity 600 c/mmole) was purchased from Collaborative Research.…”

Section: Drugsmentioning

confidence: 99%

Interaction between cyclic adenosine monophosphate and cyclic gunaosine monophosphate in guinea pig ventricular myocardium.

Watanabe¹,

Besch²

1975

Circulation Research

229

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The purpose of this study was to examine the mechanisms underlying adrenergiccholinergic antagonism in ventricular myocardium. Myocardial contractility, cyclic adenosine monophosphate (AMP) levels, and cyclic guanosine monophosphate (GMP) levels were measured in isolated guinea pig ventricles after treatment with various inotropic agents given alone and simultaneously with acetylcholine. Acetylcholine alone markedly elevated cyclic GMP levels but did not substantially change myocardial contractility. However, the same concentration of acetylcholine significantly attenuated the inotropic effect of isoproterenol and histamine, two drugs that may act by increasing myocardial levels of cyclic AMP. The decrease in the inotropic response to isoproterenol did not appear to be due to a decrease in the generation of cyclic AMP, because cyclic AMP levels were similar in hearts receiving isoproterenol alone and those receiving isoproterenol with acetylcholine. Dibutyryl cyclic GMP also antagonized the inotropic action of isoproterenol. Acetylcholine did not alter the inotropic effects of ouabain, an agent that increases myocardial contractility without changing cyclic AMP levels. These results suggest that cyclic GMP mediates the antiadrenergic effects of acetylcholine by specifically antagonizing the inotropic actions of cyclic AMP.• Histological studies done since the early 1960s have documented the presence of cholinergic innervation in the ventricular myocardium (1, 2). In addition, a number of physiological experiments have demonstrated that stimulation of vagal nerves or administration of cholinergic drugs can depress, although often minimally, the contractile state of the ventricle (3-7). The ventricular depressant effect of the cholinergic system appears to be enhanced in the presence of adrenergic stimulation (8-13). This complex interaction between adrenergic and cholinergic effects on the heart, in which the cholinergic depressant action is magnified during sympathetic stimulation, has been termed accentuated antagonism by Levy (14).Several studies, all done with broken cell preparations or tissue slices, have also shown that cholinergic drugs can attenuate catecholamineinduced increases in cyclic adenosine monophosphate (AMP) levels in cardiac tissues (15,16 attenuation of the amount of cyclic AMP generated has logically been proposed as the mechanism, at the subcellular level, for the antagonism between the adrenergic and the cholinergic systems. With the recent demonstration that the level of cyclic guanosine monophosphate (GMP) in the myocardium is increased after cholinergic stimulation (16,17), it became of interest to investigate whether the interaction of the adrenergic and cholinergic systems at the subcellular level of the heart is occurring between cyclic AMP and cyclic GMP. The series of experiments reported in this paper was performed with the objective of attempting to correlate the contractile state of intact ventricular muscle with induced changes in cyclic nucleotide (cyclic AMP and cycl...

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Depression of Ventricular Contractility by Stimulation of the Vagus Nerves

Cited by 31 publications

References 0 publications

Pulmonary vascular distensibility and lung compliance as modified by dextran infusion and subsequent atropine injection in normal subjects.

Pulmonary vascular distensibility and lung compliance as modified by dextran infusion and subsequent atropine injection in normal subjects.

Relationship between Heart Rate, Left Ventricular Output, and Stroke Volume in Preterm Infants during Fluctuations in Heart Rate

Interaction between cyclic adenosine monophosphate and cyclic gunaosine monophosphate in guinea pig ventricular myocardium.

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